Efficacy of Sunitinib and Radiotherapy in Genetically Engineered Mouse Model of Soft-Tissue Sarcoma

摘要: Purpose Sunitinib (SU) is a multitargeted receptor tyrosine kinase inhibitor of the vascular endothelial growth factor and platelet-derived receptors. The present study examined SU radiotherapy (RT) in genetically engineered mouse model soft tissue sarcoma (STS). Methods Materials Primary extremity STSs were generated mice. mice randomized to treatment with SU, RT (10 Gy × 2), or both (SU+RT). Changes tumor vasculature before after assessed vivo using fluorescence-mediated tomography. control treated tumors harvested extensively analyzed. Results mean fluorescence was not decreased by but 38–44% SU+RT. grew 1378 mm 3 12 days. alone delayed 56% 41%, respectively, maximal inhibition (71%) observed combination therapy. target effects confirmed loss phosphorylation alterations SU-related gene expression. Cancer cell proliferation apoptosis increased groups, synergistic effect on SU+RT group. had minimal microvessel density cell-specific apoptosis, >66% induced significant apoptosis. Conclusion inhibited STS cancer cells vasculature. also augmented efficacy RT, suggesting that this strategy could improve local STS.